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Biomedical subjects

Richard G Pearson

Publications and source records attributed to Richard G Pearson.

7 recordsLinked to original sources

Environmental variation and the predator-specific responses of tropical stream insects: effects of temperature and predation on survival and development of Australian Chironomidae (Diptera).

The threat posed by predation varies among predator species and with environmental context, and prey species often adjust their responses accordingly. We investigated such effects within an insect assemblage from a tropical Australian stream. These systems are frequently subjected to catastrophic floods, often suggested to reduce the importance of predation in streams, and invertebrate faunas are characterised by relatively broad environmental tolerances. Impacts of the hunting predator Australopelopia prionoptera (Diptera: Chironomidae) and an undescribed ambush predator from the Polycentropodidae (Trichoptera) on survival and development of two species of tubicolous Chironomidae, Echinocladius martini (Orthocladiinae) and Polypedilum australotropicus (Chironominae), were assessed in laboratory microcosms. A further experiment investigated how impacts of Australopelopia varied over a broad range of temperatures, exceeding that experienced annually by the studied populations. Neither predator impacted survivorship for E. martini, but the presence of the polycentropodid caused E. martini to spend longer as larvae and reduced adult longevity, and adult females were smaller-sized and had smaller oocytes. In contrast, both predators reduced survivorship of P. australotropicus, but only Australopelopia affected its development, causing reductions in pupal duration and oocyte size. The observed non-lethal impacts of predation reflect the threat each predator is known to pose to each prey species in situ. Impacts of predation varied little with temperature, reflecting the broad thermal tolerances of all study species. The predator-specific responses of the prey species imply that predation is a significant selective force in tropical Australian streams, although fluctuation in intensity of predation associated with flooding may limit its importance for community structure and prey diversity at larger scales. Our results indicate a more limited scope for environmental modification of predator-prey relationships in faunas characterised by broad physiological tolerances.

Animals↗

Climate change and the migration capacity of species.

In a recent paper, McLachlan et al. presented evidence that migration rates of two tree species at the end of the last glacial (c. 10-20 thousand years ago) were much slower than was previously thought. These results provide an important insight for climate-change impacts studies and suggest that the ability of species to track future climate change is limited. However, the detection of late-glacial refugia close to modern range limits also implies that some of our most catastrophic projections might be overstated.

Climate↗

Biodiversity conservation: uncertainty in predictions of extinction risk.

Thomas et al. model species-distribution responses to a range of climate-warming scenarios and use a novel application of the species-area relationship to estimate that 15-37% of modelled species in various regions of the world will be committed to extinction by 2050. Although we acknowledge the efforts that they make to measure the uncertainties associated with different climate scenarios, species' dispersal abilities and z values (predictions ranged from 5.6% to 78.6% extinctions), we find that two additional sources of uncertainty may substantially increase the variability in predictions.

Adaptation, Physiological↗

Alpha-MSH inhibits inflammatory signalling in Schwann cells.

Peripheral nervous system injury may be corrected by surgical repair, but in many cases this is not possible and will result in loss of motor and sensory function. Schwann cells provide many neurotrophic signals essential for axon regeneration and immediately after injury inflammatory cytokines are released necessary for Schwann cell de-differentiation. However, extended periods of inflammation after injury prevent Schwann cell proliferation, and therefore interventional approaches to enhance proliferation may in turn improve axon regeneration. We therefore investigated the ability of alpha-melanocyte stimulating hormone (alpha-MSH; a potent anti-inflammatory peptide) to inhibit the activation of the NF-kappaB transcription factor (required for inflammatory signalling) in cultured rat primary Schwann cells, stimulated with tumour necrosis factor-alpha (TNF-alpha) or interferon-gamma (IFN-gamma). Both cytokines activated NF-kappaB rapidly after 60 min incubation, observed as a translocation from the cytoplasm to the nucleus. alpha-MSH inhibited activation (i.e. inhibited nuclear translocation) in response to TNF-alpha or IFN-gamma by 81% and 100% respectively. The anti-inflammatory properties of this peptide may therefore have potential for treatment of peripheral nerve injury to improve the healing response.

Animals↗

Alpha-MSH inhibits inflammatory signalling in olfactory ensheathing cells.

Alpha-melanocyte stimulating hormone (alpha-MSH) was originally documented as a peptide that induced pigmentation in skin. However, more recent work suggests that it acts as a potent anti-inflammatory molecule in several tissues including nerve. Alpha-MSH works by directly inhibiting cytokines that cause inflammation, in particular tumour necrosis factor-alpha, interleukin-1beta, interleukin-6 and gamma-interferon. A common mechanism of inhibition is via the NF-kappaB transcription factor. We investigated the ability of alpha-MSH to inhibit the activation of NF-kappaB in cultured rat primary olfactory ensheathing cells stimulated with tumour necrosis factor-alpha or gamma-interferon. Both cytokines activated NF-kappaB rapidly (after 60 min incubation), observed as a translocation from cytoplasm to nucleus. alpha-MSH inhibited this activation (and hence nuclear translocation) by approximately 50% for both cytokines. The anti-inflammatory properties of this peptide in neural cells may therefore support a basis for treating CNS injury, where inflammation is a major problem.

Animals↗

Spatial confinement of neurite regrowth from dorsal root ganglia within nonporous microconduits.

Tissue engineering is founded on the concept of controlling the behavior of individual cells to stimulate tissue formation. This control is achieved by mimicking signals that manage natural tissue development or repair. These interdependent signals include cytokine delivery, extracellular matrix interactions, and cell-cell communication. Here, we report on the effect of spatial guidance as a signal for nerve tissue regeneration, using a simple in vitro model. We observe the acceleration of neurite extension from rat dorsal root ganglia within micron-scale tubes. Within these hydrogel-filled conduits, neurites were observed to extend more rapidly than when cultured within the hydrogel alone. The spatial cue also induced a change in tissue architecture, with the cabling of cells within the microconduit. The acceleration of neurite extension was found to be independent of conduit diameter within the range of 200 to 635 microm. Finally, our in vitro model enabled quantification of the effect of combining spatial control and localized nerve growth factor delivery.

Animals↗